Myocardial apoptosis and mesenchymal stem cells with acute exercise.

Physiological reports (2017-06-04)
Maria F Arisi, Erica N Chirico, Roxanne Sebeny, Geetha Muthukumaran, Anbin Mu, Bart C De Jonghe, Kenneth B Margulies, Joseph R Libonati

Aerobic exercise confers many health benefits. However, numerous reports have shown that acute aerobic exercise can injure the heart. We tested the general hypothesis that acute moderate-intensity exercise in rodents induces cardiomyocyte damage and stimulates mesenchymal stem cells (MSCs) to increase paracrine-mediated protective effects on cardiomyocytes. A single session of treadmill running (13 m/min, 0% grade, for 45 min) in untrained C57BL/6 male mice (n = 18) increased cleaved poly ADP-ribose polymerase (PARP), a marker of apoptosis, in the myocardium 24 h postexercise. Microarray analysis of mouse myocardium identified 11 relevant apoptotic genes and several shifts in matrix remodeling transcripts over the postexercise window. Postexercise cardiomyocyte death was recapitulated in neonatal rat cardiomyocytes (NRCMs) by culturing cells in 2% plasma harvested from exercised rats. The increased cell death observed in exercise-treated NRCMs was attenuated by β-adrenergic blockade, but not antioxidant treatment. MSC survival, proliferation, and chemotaxis showed no significant differences between sedentary and exercise plasma conditions, despite increased IL-6, TNF-α, IL-1β, and IFN-γ secretions from MSCs treated with exercise plasma. NRCM survival was increased nearly 500% when cocultured with MSCs, but this effect was not altered under exercise plasma culture conditions. Our results suggest acute moderate-intensity aerobic treadmill running in exercise-naïve rodents induces temporal cardiomyocyte death due to plasma-borne factors, namely, catecholaminergic stress. Even though exercise conditions prompt an inflammatory response in MSCs, the exercise milieu does not alter the MSC-protective phenotype on cardiomyocytes.

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D-α-Tocopherol succinate, semisynthetic, 1210 IU/g

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